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In the Original Article, the eleventh author name was published incorrectly. The correct author name is Milica Pejovic-Milovancevic. The original article has been corrected. © 2021, Springer-Verlag GmbH Germany, part of Springer Nature.

In the original articles, the last four members’ of COVID-19 Child and Adolescent Psychiatry Consortium affiliation were incorrectly published. The correct affiliation are given below. Nihal Yurteri: Department of Child and Adolescent Psychiatry, Faculty of Medicine, Düzce University, Düzce, Turkey Florian Daniel Zepf: Department of Child and Adolescent Psychiatry, Psychosomatic Medicine and Psychotherapy, Jena University Hospital, Friedrich Schiller University Jena, Jena, Germany Anna Zielinska-Wieniawska: Department of Child and Adolescent Psychiatry, Medical University of Warsaw, Warsaw, Poland Alessandro Zuddas: Department of Biomedical Science and “G. Brotzu” Hospital Trust, Child and Adolescent Neuropsychiatry, University of Cagliari, Cagliari, Italy The original article has been corrected. © 2021, Springer-Verlag GmbH Germany, part of Springer Nature.

The 22q11.2 deletion syndrome (22q11DS) is associated with a 20-25% risk of schizophrenia. In a cohort of 962 individuals with 22q11DS, we examined the shared genetic basis between schizophrenia and schizophrenia-related early trajectory phenotypes: sub-threshold symptoms of psychosis, low baseline intellectual functioning and cognitive decline. We studied the association of these phenotypes with two polygenic scores, derived for schizophrenia and intelligence, and evaluated their use for individual risk prediction in 22q11DS. Polygenic scores were not only associated with schizophrenia and baseline intelligence quotient (IQ), respectively, but schizophrenia polygenic score was also significantly associated with cognitive (verbal IQ) decline and nominally associated with sub-threshold psychosis. Furthermore, in comparing the tail-end deciles of the schizophrenia and IQ polygenic score distributions, 33% versus 9% of individuals with 22q11DS had schizophrenia, and 63% versus 24% of individuals had intellectual disability. Collectively, these data show a shared genetic basis for schizophrenia and schizophrenia-related phenotypes and also highlight the future potential of polygenic scores for risk stratification among individuals with highly, but incompletely, penetrant genetic variants.Polygenic risk scores are nearing a level of differentiation required for their clinical utility in risk prediction in populations with high-risk rare pathogenic genetic variants.

© 2017 The Authors. Background - The 22q11.2 deletion syndrome (22q11.2DS; DiGeorge syndrome/velocardiofacial syndrome) occurs in 1 of 4000 live births, and 60% to 70% of affected individuals have congenital heart disease, ranging from mild to severe. In our cohort of 1472 subjects with 22q11.2DS, a total of 62% (n=906) have congenital heart disease and 36% (n=326) of these have tetralogy of Fallot (TOF), comprising the largest subset of severe congenital heart disease in the cohort. Methods and Results - To identify common genetic variants associated with TOF in individuals with 22q11.2DS, we performed a genome-wide association study using Affymetrix 6.0 array and imputed genotype data. In our cohort, TOF was significantly associated with a genotyped single-nucleotide polymorphism (rs12519770, P=2.98×10-8) in an intron of the adhesion GPR98 (G-protein-coupled receptor V1) gene on chromosome 5q14.3. There was also suggestive evidence of association between TOF and several additional single-nucleotide polymorphisms in this region. Some genome-wide significant loci in introns or noncoding regions could affect regulation of genes nearby or at a distance. On the basis of this possibility, we examined existing Hi-C chromatin conformation data to identify genes that might be under shared transcriptional regulation within the region on 5q14.3. There are 6 genes in a topologically associated domain of chromatin with GPR98, including MEF2C (Myocyte-specific enhancer factor 2C). MEF2C is the only gene that is known to affect heart development in mammals and might be of interest with respect to 22q11.2DS. Conclusions - In conclusion, common variants may contribute to TOF in 22q11.2DS and may function in cardiac outflow tract development.

INTRODUCTION Velocardiofacial syndrome (VCFS) is a neurogenetic disorder caused by a microdeletion on chromosome 22q11. Among other cognitive impairments and learning difficulties affected individuals show difficulties in estimating time intervals (Debbané et al. 2005). Interestingly neuroimaging studies have found an increased volume of the basal ganglia of people with VCFS (Eliez et al. 2002; Kates et al. 2004; Campbell et al. 2006). Given that the caudate nucleus represents a central component of the cerebral network underlying temporal perception skills the present report proposes to examine potential relationships between cerebral alteration to the caudate nucleus and time estimation in individuals with VCFS. METHODS A group of 30 patients with VCFS and 38 age matched healthy individuals participated in time perception and time reproduction tasks. In the time perception task individuals listened to two sequential stimuli and had to choose the longer of both stimuli by pressing a button. In the time reproduction task subjects listened to a succession of sounds and once this succession had stopped they had to reproduce the same rhythm with their dominant index. Cerebral MRI images were also obtained for each participant. A manual tracing procedure was performed to measure the basal ganglia volume. RESULTS Participants with VCFS demonstrated significantly poorer performances during the time perception and time reproduction tasks in comparison to the control participants. Further increased volume of the caudate nucleus was found in individuals with VCFS. Correlational analyses revealed a significant relationship between the caudate nucleus's volume and the performances obtained in the time perception task for control participants. This correlation was not found for individuals with VCFS. CONCLUSION The present results suggest that cerebral alterations to the caudate nucleus in VCFS may alter the temporal perception function it sustains.

22q11.2 deletion syndrome (22q11DS), most frequently caused by a de novo microdeletion on the long arm of chromosome 22, is one of the most common neurogenetic syndromes. The cognitive and behavioral characteristics associated with the 22q11.2 phenotype can be quite heterogeneous, part of the reason the syndrome is often detected very late, if at all. Though in individuals with more severe cardiac, respiratory, or speech and language problems, 22q11DS is more easily detected at a young age. The cognitive profile in 22q11DS varies between borderline IQ and mild mental retardation. Less than half children have mental retardation but a majority suffer from learning difficulties. It is also typically characterized by a verbal-visual dissociation, with verbal abilities higher than visuo-spatial and abstract reasoning. Psychiatric comorbidity is also frequent in 22q11DS, and the presence of psychotic symptoms in pre-adolescence may be unique to the syndrome. In older adolescents and young adults, social withdrawal often becomes more intense and can be an indicator of psychiatric disorder. Neuroimaging studies in 22q11DS indicate different patterns of structural alterations in affected children and adults that directly relate to cognitive impairments in the syndrome. For these reasons, we believe that treatment of persons affected by 22q11DS should include periodic evaluations and frequent clinical check-ups that integrate recommendations for medical, speech, psychiatric, and academic problems.